Key Laboratory of Trace Element Nutrition of National Health Commission of China, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, 27 Nanwei Road, Beijing 100050, China.
Key Laboratory of Trace Element Nutrition of National Health Commission of China, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, 27 Nanwei Road, Beijing 100050, China.
J Trace Elem Med Biol. 2020 Dec;62:126575. doi: 10.1016/j.jtemb.2020.126575. Epub 2020 Jun 17.
KIO and KI are the most common salt iodization agents. Coincidentally, iodine exists naturally in high-iodine drinking water in the form of iodide (I) or iodate (IO). As an oxidizing substance, IO should be reduced to I before it can be effectively used by the thyroid. However, there is a lack of systematic studies on the metabolic process of high dose KIOin vivo.
The iodine metabolism processes in the thyroid and serum of rats after high KIO intake were determined using high-performance liquid chromatography-inductively coupled plasma-mass spectrometry (HPLC/ICP-MS) and arsenic cerium catalytic spectrophotometry. The changes of redox activity in the serum, thyroid, liver, and kidneys were observed by detecting total antioxidative activity (TAA).
High doses of IO were completely reduced to Iin vivo within 0.5 h. The level of organic bound iodine in the serum was stable, while the organic bound iodine in the thyroid increased to a plateau after intake of high-dose KIO. The levels of total iodine and I in serum and thyroid increased quickly, then all decreased after reaching the maximum absorption peak, and I had two absorption peaks in serum. The thyroid blocking dose of I was 0.5 mg/kg in rat. Additionally, high KIO intake did not influence the TAA in serum and other tissues.
The body is able to reduce and utilize high doses of KIO ingested through the digestive tract. The metabolism of high KIOin vivo is characterized by two absorption process of I in serum and the thyroid blocking effect. Moreover, a single intake of high-dose KIO does not affect TAA in vivo. The results suggest that such excess IO may have be reduced in the digestive tract before I enters the blood.
KIO 和 KI 是最常用的碘盐化剂。巧合的是，碘以碘化物 (I) 或碘酸盐 (IO) 的形式存在于高碘饮用水中。作为一种氧化物质，IO 应该在被甲状腺有效利用之前还原为 I。然而，目前缺乏关于高剂量 KIO 在体内代谢过程的系统研究。
采用高效液相色谱-电感耦合等离子体质谱法 (HPLC/ICP-MS) 和砷铈催化分光光度法，研究大鼠摄入高剂量 KIO 后甲状腺和血清中的碘代谢过程。通过检测总抗氧化活性 (TAA) 观察血清、甲状腺、肝脏和肾脏中氧化还原活性的变化。
高剂量的 IO 在体内 0.5 h 内完全还原为 I。血清中有机结合碘的水平保持稳定，而摄入高剂量 KIO 后甲状腺中有机结合碘增加到一个平台。血清和甲状腺中总碘和 I 的水平迅速增加，达到最大吸收峰后均下降，血清中 I 有两个吸收峰。大鼠的碘阻断剂量为 0.5mg/kg。此外，高 KIO 摄入不影响血清和其他组织中的 TAA。
机体能够还原并利用通过消化道摄入的高剂量 KIO。体内高 KIO 的代谢特征是血清和甲状腺中 I 的两个吸收过程以及甲状腺阻断作用。此外，单次摄入高剂量 KIO 不会影响体内 TAA。结果表明，这种过量的 IO 可能在 I 进入血液之前在消化道中被还原。
